Next Article in Journal
Detection and Cellular Tropism of Porcine Astrovirus Type 3 on Breeding Farms
Previous Article in Journal
HBV Reactivation in Patients Undergoing Hematopoietic Stem Cell Transplantation: A Narrative Review
Open AccessArticle

The Capsid Protein of Hepatitis E Virus Inhibits Interferon Induction via Its N-Terminal Arginine-Rich Motif

1
Molecular Virology Laboratory, VA-MD College of Veterinary Medicine and Maryland Pathogen Research Institute, University of Maryland, College Park, MD 20740, USA
2
Department of General Practice, Nanjing Medical University, Nanjing 210006, China
3
College of Veterinary Medicine, Northeast A&F University, Yangling 712100, China
*
Author to whom correspondence should be addressed.
Viruses 2019, 11(11), 1050; https://doi.org/10.3390/v11111050
Received: 22 October 2019 / Accepted: 7 November 2019 / Published: 11 November 2019
(This article belongs to the Section Animal Viruses)
Hepatitis E virus (HEV) causes predominantly acute and self-limiting hepatitis. However, in HEV-infected pregnant women, the case fatality rate because of fulminant hepatitis can be up to 30%. HEV infection is zoonotic for some genotypes. The HEV genome contains three open reading frames: ORF1 encodes the non-structural polyprotein involved in viral RNA replication; ORF2 encodes the capsid protein; ORF3 encodes a small multifunctional protein. Interferons (IFNs) play a significant role in the early stage of the host antiviral response. In this study, we discovered that the capsid protein antagonizes IFN induction. Mechanistically, the capsid protein blocked the phosphorylation of IFN regulatory factor 3 (IRF3) via interaction with the multiprotein complex consisting of mitochondrial antiviral-signaling protein (MAVS), TANK-binding kinase 1 (TBK1), and IRF3. The N-terminal domain of the capsid protein was found to be responsible for the inhibition of IRF3 activation. Further study showed that the arginine-rich-motif in the N-terminal domain is indispensable for the inhibition as mutations of any of the arginine residues abolished the blockage of IRF3 phosphorylation. These results provide further insight into HEV interference with the host innate immunity. View Full-Text
Keywords: hepatitis E virus (HEV), interferon (IFN), the capsid protein; arginine-rich motif; IRF3 phosphorylation hepatitis E virus (HEV), interferon (IFN), the capsid protein; arginine-rich motif; IRF3 phosphorylation
Show Figures

Figure 1

MDPI and ACS Style

Lin, S.; Yang, Y.; Nan, Y.; Ma, Z.; Yang, L.; Zhang, Y.-J. The Capsid Protein of Hepatitis E Virus Inhibits Interferon Induction via Its N-Terminal Arginine-Rich Motif. Viruses 2019, 11, 1050.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop